SUMMARY OF WORK. This research investigates physiological mechanisms by which stress and high sodium intake contribute to the pathogenesis of hypertension. Experimental studies with laboratory animals found that aversive behavioral conditioning paradigms that decreased breathing frequency and increased pCO2 also decreased renal sodium excretion. In combination with sodium loading, these procedures resulted in progressive hypertension over days and weeks. Related studies with healthy humans showed that voluntary hypopnic breathing also decreased renal sodium excretion and increased plasma concentrations of natriuretic hormones that are sensitive to expansion of plasma volume. Subsequently, high resting end tidal CO2 was found to be a risk factor for blood pressure sensitivity to high dietary sodium intake. Over the past year, studies with participants in the Baltimore Longitudinal Study on Aging have found that (a) women (but not men) who report high perceived stress breathe more slowly at rest than those who report low perceived stress, (b) men and women who breathe slowly at rest maintain higher levels of resting end tidal CO2, and (c) women (but not men) who maintain high resting end tidal CO2 have higher resting systolic blood pressure, particularly if they suppress expression of anger. Taken together, these studies support the view that chronic inhibition of breathing can influence the effects of high dietary sodium intake on resting blood pressure, and participate in some forms of chronic hypertension. Studies are needed to determine the origins of the gender differences in the associations of emotions, inhibited breathing pattern and blood pressure.